Analysis of the growth hormone (GH) gene in 12 strains of White Leghorn chickens revealed restriction fragment length polymorphisms (RFLPs) at three MspI sites and at a SacI site. Based on linkage disequilibrium analysis, they gave rise to eight different alleles (i.e. combinations of RFLPs), with five occurring at frequencies above 5% in at least one strain. Pairs of GH-RFLPs were at near maximal linkage disequilibrium, suggesting either a lack of recombination or the presence of selection pressure during evolution of the GH gene. Allele frequencies were determined in 12 non-inbred strains derived from three different genetic bases. These strains had been selected either for an array of egg production traits, resistance to Marek's disease or resistance to avian leukosis. Selection for disease resistance was consistently correlated with an increase in the frequency of one of the alleles. One strain segregated for only two alleles, which differed by three RFLPs. Analysis of variance in this strain indicated that the GH allele co-selected with resistance was associated with a delayed onset of ovulation but a higher persistency of ovulation as age progressed, resulting in an overall increase of egg production by 15% (age at first egg to 497 days). The resistance-associated GH allele was dominant for the onset of ovulation and recessive for the persistency of egg production. There was no significant effect of the GH genotype on juvenile body weight, egg weight or egg specific gravity.
By serum typing, it is indicated that HLA B27 may be associated with the susceptibility to ankylosing spondylitis (AS). We analyzed DNA restriction fragment length polymorphism (RFLP) in 28 Chinese AS patients and 99 healthy controls, using a 1.4 Kb HLA class I cDNA probe. The results showed that the frequencies of the 8.1 Kb EcoRI, 5.2 Kb EcoRI and 21.9 Kb XbaI fragments were found to be significantly increased in affected patients (P less than 0.0001, P = 0.0015, respectively), but that of 19.2 Kb XbaI fragment was decreased (P = 0.0021). The data suggest that AS may be a polygenic disease; furthermore, B27 and 8.1 Kb EcoRI band may be two different factors responsible for the susceptibility or just in linkage disequilibrium with the susceptible gene(s).
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